Experimental Models of Surgical Inflammation
Pp. 309-343 (35)
Maria-Angeles Aller, Natalia de las Heras, Natalia Arias, Isabel Prieto, Laureano Lorente, Maria-Paz Nava, Luis Santamaria, Jorge-Luis Arias, Vicente Lahera and Jaime Arias
Prehepatic portal hypertension induces a splanchnic low-grade inflammatory
response that could switch to high-grade inflammation with the development of severe
and life-threatening complications when associated with chronic liver disease. The
extraembryonic origin of the portal system may determine the regression to an
extraembryonic phenotype i.e., vitellogenic and amniotic, during the evolution of both
types of portal hypertension. Thus prehepatic portal hypertension, or compensated
hypertension by portal vein ligation in the rat, is associated with molecular mechanisms
related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out.
In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or
decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic
interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to
create an inflammatory pathway that could have a key pathophysiological relevance in
the production of ascites. The hypothetical comparison between the ascitic and the
amniotic fluid also allows for translational investigation. The induced regression of the
splanchnic system to extraembryonic functions by portal hypertension highlights the
great relevance of the extraembryonic structures even during post-natal life.
Portal hypertension, microsurgery, extrahepatic cholestasis, ascites,
mini-brain, high grade inflammation, fetal development, amniotic fluid, lymph
flow, hepatic steatosis, mast cell, splanchnic system.
Department of Surgery, School of Medicine, Complutense University, Ramón y Cajal Square, 28040 MADRID, Spain.